Low-dose mercury heightens early innate response to coxsackievirus infection in female mice
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- 作者：Kayla L. Penta ; DeLisa Fairweather ; Devon L. Shirley ; Noel R. Rose…
- 关键词：Mercury ; Innate immunity ; Cytokine ; Coxsackievirus ; Autoimmunity
- 刊名：Inflammation Research
- 出版年：2015
- 出版时间：January 2015
- 年：2015
- 卷：64
- 期：1
- 页码：31-40
- 全文大小：1,141 KB
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17. Nyland JF, Fairweather D, Shirley DL, Davis SE, Rose NR, Si - 作者单位：Kayla L. Penta (1)
DeLisa Fairweather (2)
Devon L. Shirley (1)
Noel R. Rose (3) (4)
Ellen K. Silbergeld (2)
Jennifer F. Nyland (1) (2)
1. Department of Pathology, Microbiology and Immunology, University of South Carolina, School of Medicine, 6439 Garner’s Ferry Rd, VA#1 B10, Columbia, SC, 29208, USA
2. Department of Environmental Health Sciences, Johns Hopkins University Bloomberg School of Public Health, Baltimore, USA
3. W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, USA
4. Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, USA - 刊物类别：Biomedical and Life Sciences
- 刊物主题：Biomedicine
Immunology
Pharmacology and Toxicology
Allergology
Dermatology
Neurology
Rheumatology - 出版者：Birkh盲user Basel
- ISSN：1420-908X
文摘
Objective Mercury is a ubiquitous environmental contaminant with toxic outcomes over a range of exposures. In this study, we investigated the effects of mercury exposure on early immune responses to coxsackievirus B3 (CVB3) infection in a murine model of autoimmune heart disease. Materials and methods Female BALB/c mice, susceptible to CVB3-induced autoimmune myocarditis, were treated with mercuric chloride (200?μg/kg body weight every other day for 2?weeks) prior to infection with CVB3. Six hours post-infection, immune cells were isolated from the spleen and peritoneum for flow cytometry, gene expression, and cytokine profiling. Thirty-five days post-infection, hearts were collected for histological examination of immune cell infiltration. Results As for male mice, mercury exposure significantly increased autoimmune myocarditis and immune infiltration into the heart. During the innate response 6?h post-infection, mercury increased expression of co-stimulatory molecules and innate immune receptors on peritoneal macrophages. At the same time point, the alternatively activated macrophage gene, arginase, was increased while the classically activated macrophage gene, inducible nitric oxide synthase, was unaffected. Expression of activation markers were decreased on peritoneal B cells with mercury exposure while T cells were unaffected. Mercury increased production of pro-inflammatory mediators in the spleen. Macrophage-recruiting chemokines and activating cytokines, such as CCL2, CCL4, and IL-6, were increased with mercury following CVB3 infection. Conclusions Thus, mercury treatment exacerbates autoimmune myocarditis in female mice and alters early innate signaling on peritoneal macrophages. Mercury also modulates the cytokine profile in the spleen toward a macrophage-activating milieu, and upregulates alternatively activated macrophage genes, providing evidence that mercury exposure promotes inflammation in the context of infection.